In recent years there has been increasing evidence in the literature that pituitary hormones are capable of regulating the immune system. There is evidence to suggest that prolactin is an immunostimulatory hormone and that reduction of serum prolactin levels in experimental animals by hypothesectomy or bromocriptine will result in a degree of immunosuppression. An animal model of experimental autoimmune uveitis (EAU) induced by immunization of rats with S-antigen (a soluble antigen from the retina) is used as a model for intraocular inflammatory disease. We have demonstrated that concurrent antibody production in both males and females and the incidence of uveitis in female animals but did not have a significant effect on the immune responses measured by lymphocyte proliferation. As reported before, cyclosporine in high doses (10 mg/kg) there is only partial effect. We have demonstrated that the concurrent use of bromocriptine to suppress prolactin in combination with low dose cyclosporine is more effective than either drug separately in suppressing both the incidence of disease as well as the cellular and humoral immune responses to immunization. There is evidence in the literature to suggest that cyclosporine is able to compete for binding on the lymphocyte by prolactin and that reductions in prolactin level may therfore make cyclosporine more effective. Further studies in animal disease will hopefully elucidate other aspects of the neuroendocrine axis which can be utilized to regulate the immune system to treat autoimmune diseases.